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      Central sensitization: a biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome

      review-article
      1 , 2 , 1 , 2 , 3 ,
      Clinical Rheumatology
      Springer-Verlag
      Central sensitization, Chronic fatigue syndrome, Chronic pain, Fibromyalgia

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          Abstract

          In addition to the debilitating fatigue, the majority of patients with chronic fatigue syndrome (CFS) experience chronic widespread pain. These pain complaints show the greatest overlap between CFS and fibromyalgia (FM). Although the literature provides evidence for central sensitization as cause for the musculoskeletal pain in FM, in CFS this evidence is currently lacking, despite the observed similarities in both diseases. The knowledge concerning the physiological mechanism of central sensitization, the pathophysiology and the pain processing in FM, and the knowledge on the pathophysiology of CFS lead to the hypothesis that central sensitization is also responsible for the sustaining pain complaints in CFS. This hypothesis is based on the hyperalgesia and allodynia reported in CFS, on the elevated concentrations of nitric oxide presented in the blood of CFS patients, on the typical personality styles seen in CFS and on the brain abnormalities shown on brain images. To examine the present hypothesis more research is required. Further investigations could use similar protocols to those already used in studies on pain in FM like, for example, studies on temporal summation, spatial summation, the role of psychosocial aspects in chronic pain, etc.

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          Neuronal plasticity: increasing the gain in pain.

          We describe those sensations that are unpleasant, intense, or distressing as painful. Pain is not homogeneous, however, and comprises three categories: physiological, inflammatory, and neuropathic pain. Multiple mechanisms contribute, each of which is subject to or an expression of neural plasticity-the capacity of neurons to change their function, chemical profile, or structure. Here, we develop a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain, identifying distinct forms of plasticity, which we term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.
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            Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence.

            Peripheral tissue damage or nerve injury often leads to pathological pain processes, such as spontaneous pain, hyperalgesia and allodynia, that persist for years or decades after all possible tissue healing has occurred. Although peripheral neural mechanisms, such as nociceptor sensitization and neuroma formation, contribute to these pathological pain processes, recent evidence indicates that changes in central neural function may also play a significant role. In this review, we examine the clinical and experimental evidence which points to a contribution of central neural plasticity to the development of pathological pain. We also assess the physiological, biochemical, cellular and molecular mechanisms that underlie plasticity induced in the central nervous system (CNS) in response to noxious peripheral stimulation. Finally, we examine theories which have been proposed to explain how injury or noxious stimulation lead to alterations in CNS function which influence subsequent pain experience.
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              A community-based study of chronic fatigue syndrome.

              Most previous estimates of the prevalence of chronic fatigue syndrome (CFS) have derived largely from treated populations, and have been biased by differential access to health care treatment linked with sex, ethnic identification, and socioeconomic status. To assess the point prevalence of CFS in an ethnically diverse random community sample. A sample of 28,673 adults in Chicago, Ill, was screened by telephone, and those with CFS-like symptoms were medically evaluated. MAIN OUTCOME MEASURES AND ANALYSES: Self-report questionnaires, psychiatric evaluations, and complete medical examinations with laboratory testing were used to diagnose patients with CFS. Univariate and multivariate statistical techniques were used to delineate the overall rate of CFS in this population, and its relative prevalence was subcategorized by sex, ethnic identification, age, and socioeconomic status. There was a 65.1% completion rate for the telephone interviews during the first phase of the study. Findings indicated that CFS occurs in about 0.42% (95% confidence interval, 0.29%-0.56%) of this random community-based sample. The highest levels of CFS were consistently found among women, minority groups, and persons with lower levels of education and occupational status. Chronic fatigue syndrome is a common chronic health condition, especially for women, occurring across ethnic groups. Earlier findings suggesting that CFS is a syndrome primarily affecting white, middle-class patients were not supported by our findings.
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                Author and article information

                Contributors
                +32-3-6418205 , jo.nijs@vub.ac.be
                Journal
                Clin Rheumatol
                Clinical Rheumatology
                Springer-Verlag (London )
                0770-3198
                1434-9949
                18 November 2006
                April 2007
                : 26
                : 4
                : 465-473
                Affiliations
                [1 ]Department of Human Physiology, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel (VUB), Brussel, Belgium
                [2 ]Division of Musculoskeletal Physiotherapy, Department of Health Sciences, University College Antwerp, Antwerp, Belgium
                [3 ]Department of Health Sciences, Division of Musculoskeletal Physiotherapy, Hogeschool Antwerpen (HA), Van Aertselaerstraat 31, 2170 Merksem, Belgium
                Article
                433
                10.1007/s10067-006-0433-9
                1820749
                17115100
                0d5354f3-52b6-4e8a-a5e5-d72b3f490f7a
                © Clinical Rheumatology 2006
                History
                : 20 June 2006
                : 28 August 2006
                : 31 August 2006
                Categories
                Review
                Custom metadata
                © Clinical Rheumatology 2007

                Rheumatology
                central sensitization,fibromyalgia,chronic pain,chronic fatigue syndrome
                Rheumatology
                central sensitization, fibromyalgia, chronic pain, chronic fatigue syndrome

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